Chronic obstructive pulmonary disease (COPD) means a wide variety of groups of lung diseases impeding normal breathing and is a disease of lung obstruction by the presence of at least one disease selected from asthma, pulmonary emphysema and chronic bronchitis. COPD is such that these diseases frequently co-exist at the same time and a difficulty is involved in confirming whichever disease is a cause bringing about lung obstruction in individual diseases. In clinical aspect, COPD has been diagnosed by a lowering of an expiratory flow rate from the lungs, which is kept constant over several months and which continuously continues over two years in cases of chronic bronchitis. The two most serious states related with COPD include chronic bronchitis and pulmonary emphysema.
Of these, pulmonary emphysema means a state where an abnormal enlargement develops bringing about the destruction of tissues called pulmonary alveolar parenchyma such as of alveolar bronchioles, pulmonary alveoli, alveolar sacs or the like serving as a gas exchange site. Although the pulmonary alveolar parenchyma in its normal state shrinks during expiration, emphysema-suffering pulmonary alveolar parenchyma does not return to its original state if once enlarged by breathing. Therefore, one cannot breathe well. Besides, the effective area and vascular bed (blood capillaries running randomly throughout the surfaces of the pulmonary alveoli) of the pulmonary alveoli decrease, thereby lowering the ventilatory function of the lungs as a whole. Additionally, since elastin, collagen and the like are destroyed from inflammation, the elasticity of lung lowers and it is not thus possible to expand the lung by pulling the respiratory tract open, so that the bronchi are in a condition of likelihood of deformation. Accordingly, as set out in PCT International Publication No. WO2009/075106 Pamphlet, when the lungs contract upon breathing, the bronchi thereof is narrowed by being compressed with the pulmonary alveoli filled with air, with the result that the lungs are hyperinflated, thus making it difficult to release the air. To cope with this, as set out, for example, in [Jadranka Spahija et al., “Effects of Imposed Pursed-Lips Breathing on Respiratory Mechanics and Dyspnea at Rest and During Exercise in COPD,” Chest 2005; 128:640-650], patients with pulmonary emphysema exhale through pursed-lips breathing so as to breathe out air.
In Japan, about 50,000 persons suffer this disease and have now undergone home oxygen therapy. It is said that when including those persons having a mild disease condition, about three million persons are regarded as backup candidates for pulmonary emphysema. For the therapy, the home oxygen therapy is main treatment at present. The oxygen therapy has been frequently used in a condition where sufficient oxygen cannot be absorbed from air because pulmonary function is severely impaired. However, this therapy merely alleviates symptoms and is thus not an effective treatment. For drug therapy, for example, mention is made of: a method wherein a bronchodilator is used to help keep the airways in the lungs open thereby alleviating the shortness of breath as described in [Jan A. van Noord et al., “Effects of Tiotropium With and Without Formoterol on Airflow Obstruction and Resting Hyperinflation in Patients with COPD,” Chest 2006; 129: 509-517]; a method of reducing inflammation in the airways by use of an inhaled steroid drug or peroral steroid drug; a method of preventing and treating additional inflammation by use of antibiotics; and a method of eliminating the mucus from the airways by using an expectorator.
However, as described in [Ware J H, et al., “Cost effectiveness of Lung-Volume-Reduction Surgery for Patients with Sever Emphysema,” The new England Journal of Medicine 2003; 348:2005-2056] and also in [National Emphysema Treatment Trial Research Group, “A Randomized Trial Comparing Lung-Volume-Reduction Surgery with Medical Therapy for Severe Emphysema,” The new England Journal of Medicine 2003; 348:2059-2073], all these drug therapies help control the pulmonary emphysema and alleviate the symptoms, but are not an effective treatment. In addition, there are known a surgical therapy such as a lung reduction operation wherein the damaged portion of lung is removed to allow a normal part of lung to be enlarged, and lung transplantation. However, these methods would impose a great burden on patients and it is difficult to secure a lung substitute.
If lung volume reduction (LVR) can be non-invasively achieved without thoracotomy, there can be given a chance for treatment of more patients. Nevertheless, the success rate of the existing non-invasive treatment is low. For the non-invasive treatment, there is known an apparatus of impeding an inspiration inflow toward the terminal direction of lung by indwelling a structure having a unidirectional valve mechanism inside the bronchus so as to obtain similar effects to the lung volume reduction surgery (LVRS) as set forth, for example, in the U.S. Pat. No. 6,258,100 specification. However, in case where these structures have been indwelled, there is pointed out, in the U.S. Pat. No. 7,549,984, a problem in that easy access to ahead of the structures becomes difficult.
It is known that in the destroyed alveolar bronchiole or pulmonary alveolar parenchyma, there exists an air flow path called collateral channel and different from the main airway. Accordingly, as described in the Publication of United States Patent Application No. 2006/0264772, the air flow passing through the main airway can be impeded by means of the structure. Nevertheless, where collateral channels exist, air arrives at the inside of the destroyed alveolar bronchiole or pulmonary alveolar parenchyma while taking a detour path around the block with the structure, so that the lung enlargement cannot be prevented.
For a measure of achieving non-surgical lung volume reduction, there is disclosed, in Patent Document 5, a method of realizing LVR wherein a region of lung is collapsed and part of the collapsed region is bonded to other region to promote desmoplasia in the bonded tissues or therearound. In this method, however, the collapse of the pulmonary alveolar parenchyma by vital reaction has to be waited. Moreover, in the U.S. Pat. No. 6,682,520 specification, a trial method of LVR is described using a material containing a site of targeting damaged lung tissues. However, the U.S. Pat. No. 7,678,767 indicates that this method not only needs the targeting site, but also needs a process of reaction with the damaged site. Hence, an effective treating method of pulmonary emphysema is not now known in this field.
The disease state where pulmonary emphysema is an underlying disease like COPD includes pneumothorax. The pneumothorax is a disease state where a hole is made in the visceral pleura surrounding the lung per se and air is leaked into a space inside the lung inbetween with the visceral pleura at the side of thorax.
Where breathing is prevented by pneumothorax, there is performed a drainage method wherein a tube is inserted through an incision in the chest wall and the air inbetween the parietal pleura and the visceral pleura is drained, or a resection treatment of cystectomy under thoracoscopy. However, with the drainage method, it takes several or more days for healing and the treatment under thoracoscopy is a sort of operation, with high invasiveness on the part of patient. The pneumothorax is high in rate of recurrence and thus, there have been demanded a shortage in time required for one treatment and a reduction in operation invasiveness.